Abstract

Ionotropic glutamate receptors mediate excitatory synaptic transmission at most central mammalian synapses. In addition to converting the chemical signal released from the presynaptic terminal to an electrical response in the postsynaptic neuron, these receptors are critically involved in activity-dependent, long-term changes in synaptic strength and, therefore, are central to processes thought to underlie learning and memory. Several mechanisms have been proposed to play roles in altering synaptic strength, and it is clear that there are several different forms of long-term synaptic plasticity in the mammalian brain. Here, we review recent evidence that some forms of synaptic strengthening rely on the modification of the glutamate receptor complement at synapses in response to activity-dependent processes.